Related Experiment Video
Updated: Aug 23, 2026
An In Vivo Estrogen Deficiency Mouse Model for Screening Exogenous Estrogen Treatments of Cardiovascular Dysfunction After Menopause
Published on: August 13, 2019
Carotid and uterine vascular resistance in short-term hormone replacement therapy postmenopausal users
Felipe Lazar1, Lucia Costa-Paiva, Aarão Mendes Pinto-Neto
1Department of Obstetrics and Gynecology, Medical Sciences School, University of Campinas (Unicamp), R. Alexander Fleming 101, 13083-970 Campinas, SP, Brazil. flj@uol.com.br
Objective:
To compare the short-term effects of oral hormone replacement therapy (HRT) and placebo on carotid and uterine vascular impedance.
Methods:
80 postmenopausal women selected from the outpatient clinic of the Hospital Leonor Mendes de Barros in São Paulo, Brazil, were randomized to oral HRT (estradiol 2 mg/norethisterone acetate 1 mg-Kliogest(r)) or placebo. Carotid and uterine arteries pulsatility indices (PIs) were assessed by color Doppler at baseline, after 4 and 12 weeks of treatment. Seventy-six women completed the trial, 38 in each group.
Results:
The carotid PI did not decrease significantly in either group. In the uterine arteries, the drop in PI was steeper and greater for HRT women. Drops occurred despite the supposed counteracting effect of norethisterone acetate. In placebo group, there was no significant difference between 4 and 12 weeks of treatment compared with the baseline. The results did not change when analyzed in a real treatment approach.
Conclusion:
Oral continuous HRT are effective at 12 weeks in reducing impedance to flow in uterine, but not in carotid circulation. These results suggest that the effects of HRT vary by vascular site, and do not have a detectable short-term vascular effect in the carotid area.
Related Concept Videos
01:20Vascular Resistance
The primary determinants of vascular resistance are vessel diameter, blood viscosity, and vessel length. Among these, vessel diameter plays the most significant role due to the fourth power relationship described by...
01:26Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
01:31Adrenergic Antagonists: ɑ and β-Receptor Blockers
01:18Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme (ECE). Of...
01:22Heart Failure Drugs: β-Blockers
01:23Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...